Cholesterol Diet And Cvd Treatment

HDLs transport cholesterol from body tissues / cells to the liver (for breakdown / excretion); LDLs transport cholesterol from the liver to body tissues / cells; high LDL levels lead to deposition in artery walls / atherosclerosis whereas high HDL is protective

Total cholesterol is slightly above the 5.0 mmol/dm³ guideline / borderline; however HDL is high (above 1.2 mmol/dm³) which is protective; LDL is below 3.0 mmol/dm³ which is healthy / favourable HDL:LDL ratio so overall risk is low

Sufferers have high LDL from birth due to faulty LDL receptors / genetic cause; they develop atherosclerosis / CVD much earlier than the general population; this rules out lifestyle as the only explanation, showing LDL itself causes the disease

Epidemiological studies show only correlation, not causation; other risk factors (e.g. smoking, obesity, diet) may confound the relationship / cannot be fully controlled in observational studies

A statin trial is an intervention / experiment where LDL is deliberately changed; if CVD events fall in proportion, this shows that lowering LDL directly reduces CVD risk; reference to randomisation / placebo / cause and effect

Finding the BMI $$BMI=\frac{\text{mass}}{{\text{height}}^{2}}=\frac{78}{{1.72}^{2}}$$ $$BMI=\frac{78}{2.9584}=26.4{\text{ kg m}}^{-2}$$ This is above 24.9, so the person is overweight and not in the healthy range.

WHR measures abdominal / central fat (which surrounds organs / is metabolically active); BMI does not distinguish between fat and muscle so muscular individuals can be classed as overweight despite low CHD risk

Carbon monoxide binds irreversibly to haemoglobin, reducing oxygen transport / forcing heart to work harder; nicotine raises heart rate and blood pressure; chemicals in smoke damage the endothelium of arteries; this triggers atherosclerosis / plaque formation, narrowing coronary arteries

BMI of 31 indicates obesity, increasing CHD risk; WHR of 0.95 (above 0.90 cut-off) indicates harmful central / abdominal fat; weight loss through diet (reduce saturated fats and salt, increase unsaturated fats and fibre) will lower LDL and blood pressure; regular aerobic exercise raises HDL, lowers LDL, reduces resting heart rate and blood pressure; quitting smoking removes carbon monoxide and nicotine effects, allowing endothelial damage to repair over time; combined effect significantly reduces atherosclerosis and CHD risk; reference to evidence from intervention studies showing reversibility

Statins inhibit HMG-CoA reductase / the enzyme that makes cholesterol in the liver; less cholesterol made so LDL receptors take up more LDL from the blood; lower blood LDL reduces atherosclerosis / plaque formation, lowering CVD risk

Benefit — prevent dangerous blood clots / reduce risk of stroke / heart attack; Risk — increase risk of excessive bleeding from minor injury / requires regular blood monitoring (e.g. warfarin)

ACE inhibitors block conversion of angiotensin I to angiotensin II / reduce vasoconstriction; this lowers blood pressure / reduces strain on the heart; reduces risk of stroke / heart attack

Statins reliably reduce LDL by 30–50% and significantly lower CVD events in clinical trials; they work even in patients with familial hypercholesterolaemia or when lifestyle alone is not enough; however side effects include muscle pain, rare liver damage, and lifelong use is often needed; lifestyle changes (reduce saturated fat, exercise, lose weight, stop smoking) lower LDL and improve HDL with no drug side effects; lifestyle changes also benefit overall health (e.g. blood pressure, weight, diabetes risk); however adherence is often poor and harder to sustain than taking a daily pill; combination of statins and lifestyle changes is usually most effective for high-risk patients